In the two weeks following MI, monocytes / macrophages are the most represented in the ischemic heart tissue cells. The infiltration by monocytes / macrophages after infarction MI is a two-phase process. In the first phase, monocytes / macrophages M1 promote digestion injured areas, and monocytes / macrophages M2 intervene to promote angiogenesis, collagen deposition and contribute to tissue repair. The optimal repair after myocardial infarction depends on effective recruitment of monocytes and macrophages M1 transition needed to digest the damaged tissue and M2 macrophages necessary for tissue repair. The balance between these two phenotypes M1 and M2 is controlled by different modulators, such as transcription factors, cellular miRNA and miRNA extracellular contained in the microvesicles (MVs). Interestingly, plasma MVs circulating essentially derived monocytes and platelets contain miRNA and are impaired by inflammation or during various pathological situations (such as IDM). Furthermore, metabolic disorders such as hypercholesterolemia (often associated with diabetes) affect the transition from M1 to M2 response and response delay cardiac repair. To date, the mechanisms that control the M1 / M2 transition at heart level are not elucidated. Moreover, the impact of diabetes, which leads to chronic low-grade inflammation, is not explored. Targeting the immune response by promoting the transition M1 / M2 after MI could be an innovative therapeutic approach. However, better characterization of the response of M1 and M2 macrophages after MI and the mechanisms by which they contribute to tissue remodeling and the effect of diabetes are needed. The goal is to study how the phenotypes / macrophage functions after MI are changed by diabetes and to determine the potential role of miRNAs contained in secreted MVs in the transition M1 / M2 after MI.